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2015 ; 12
(3
): 4187-4195
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Reducing progression of experimental lupus nephritis via inhibition of the
B7/CD28 signaling pathway
#MMPMID26096149
Huang L
; Kong Y
; Wang J
; Sun J
; Shi Q
; Qiu YH
Mol Med Rep
2015[Sep]; 12
(3
): 4187-4195
PMID26096149
show ga
The aim of the present study was to evaluate the effects of the B7/cluster of
differentiation (CD)28 signaling pathway on experimental lupus nephritis and
examine the molecular mechanism involved by inhibiting the B7/CD28 signaling
pathway. A lupus nephritis model in C57BL/6 J mice was induced via
intraperitoneal injection of pristane. A recombinant B7?1 short hairpin RNA
(shRNA) lentivirus vector was constructed by synthesis and splicing. A
neutralizing mouse anti?human B7?1 antibody termed 4E5 was also prepared. The
mouse model of lupus nephritis was treated with B7?1 shRNA and 4E5 via injection
through the tail vein. The silencing effects of B7?1 shRNA lentiviral infection
on target molecules were evaluated using immunofluorescence and flow cytometry.
The levels of protein in the urine were detected using Albustix test paper each
month over 10 months. The concentration of interleukin (IL)?4 and interferon?? in
the serum was determined using an ELISA. The immune complex (IC) deposits in the
kidney were analyzed using direct immunofluorescence. The results demonstrated
that the C57BL/6 J mouse lupus nephritis model was successfully constructed with
immune cells activated in the spleen of the mice, increases in the concentration
of anti?nuclear antibody (ANA) and anti?double stranded DNA antibodies as well as
positive IC formation. Following B7?1 shRNA lentivirus or 4E5 treatment,
CD11b+B7?1+, CD11c+B7?1+ and CD21+B7?1+ cells in the spleen of the mice were
significantly reduced. The concentration of ANA and IL?4 in the serum was also
decreased. The concentration of urine protein was reduced and it was at its
lowest level in the 4E5 early intervention group. It was also revealed that the
immunofluorescence intensity of the IC deposits was weak in the 4E5 early
intervention group. In conclusion, inhibiting the B7?1/CD28 signaling pathway is
able to alleviate experimental lupus nephritis and provides an experimental basis
for the therapeutic use of blocking the B7?1/CD28 signaling pathway in human
lupus nephritis and other autoimmune disorders.
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